The objective of this work is to evaluate the need for creatine and phosphocreatine (CP) in skeletal muscle by evaluating the consequences of specifically depleting muscle of these compounds or of substituting another compound, such as phosphorylated beta-guanidinopropionic acid, for CP. First the specificities of creatine kinase and the membrane transport site for creatine will be compared to permit selection of the most ideal creatine antagonists. In addition, certain guanidino compounds including beta-guanidinopropionic acid will be phosphorylated, and their effects on phosphofructokinase, pyruvate kinase, glyceraldehyde-3-P dehydrogenase, and fructose-1,6-diphosphatase will be studied in vitro. Then the most promising compound(s) will be studied in vivo to evaluate their effects on creatine metabolism, on anaerobic glycolysis, on oxidative metabolism, on the function of muscle, and on the general health of rats.